Fig. 1: Paclitaxel treatment triggers inflammatory response. | Oncogenesis

Fig. 1: Paclitaxel treatment triggers inflammatory response.

From: IL-6 promotes drug resistance through formation of polyploid giant cancer cells and stromal fibroblast reprogramming

Fig. 1

A Experimental design. After treatment with paclitaxel (PTX; 500 nM) overnight (16-18 h), ovarian cancer cells, including the control cells without treatment and PGCCs induced by PTX were allowed to recover in their corresponding regular media. From recovery day 1 to 30, proinflammatory molecule levels were measured in the supernatant every 24 h. Total mRNA for sequencing was collected at recovery day 3. PGCCs collected at recovery day 7 were used for the coculture system with primary fibroblasts. B Heat map of the top 2000 genes induced by paclitaxel treatment of Hey and SKOv3 cells (control, PGCCs at recovery day 3, and daughter cells). C Up- or downregulated genes in PGCCs of Hey and SKOv3 cells (at recovery day 3) compared with the control and daughter cells. D The top up- or downregulated pathways in PGCCs compared with the control cells. E Top inflammatory molecules that were upregulated in PGCCs, among which IL-6 and IL-1β, along with CXCL3, were the predominant molecules (arrows). F Representative pictures of daughter cells (blue arrows) from mother PGCCs (red arrows, at recovery day 21). PGCCs are positive for β-gal staining (lower panels, at recovery day 21), which indicates senescence. Bars, 50 µm.

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